Latent Toxoplasma Research Articles

P.139 Cerebral toxoplasmosis in an HIV-negative patient

Background: Toxoplasma gondii is a protozoan parasite with the ability to infect any nucleated cell in humans. Most immunocompetent infected individuals are asymptomatic. Latent toxoplasma can become reactivated in immunocompromised individuals though this is exceptionally rare in HIV-negative individuals. Methods: We present the case of a 47-year-old male with chronic immunosuppression secondary to marginal zone lymphoma and steroid therapy. Results: The patient presented to hospital with a 1-week history of word-finding difficulties, intermittent right facial numbness and leg weakness, and tonic-clonic seizures. CT head showed a left temporal heterogenous mass measuring 2.8 × 2.8 × 3.5 cm. Biopsy of the lesion showed Multiple tachyzoites and rare bradyzoites with strong positivity for the toxoplasma specific immunostain. The patient was treated with trimethoprim/sulfamethoxazole which resulted in complete neurologic recovery. Conclusions: Our literature review included 32 cases of cerebral toxoplasmosis in HIV-negative patients with an overall mortality rate of 48%. Cerebral toxoplasmosis has a predilection for immunosuppressed patients with an underlying hematologic malignancy (74%, n= 23). Successful treatment requires early recognition of the disease and prompt treatment with sulfamethoxazole and trimethoprim, pyrimethamine, or sulfadiazine. Patients who recover from acute toxoplasmosis should remain on lifelong suppressive antibiotic therapy to prevent relapse.

<i>Toxoplasma Gondii</i> Bradyzoites Elicit Transcriptional Changes in Host Cells to Prevent IFNγ-Mediated Cell Death

Toxoplasma gondii bradyzoites are a chronic reservoir for disease reactivation in toxoplasmosis, which causes blindness and encephalitis. Acute-stage tachyzoites extensively manipulate their host cell by exporting a repertoire of proteins across the parasitophorous vacuolar membrane (PVM). This interferes with the hosts transcriptional program, allowing for persistence during immune attack. It is unknown how bradyzoites persist and what role host manipulation plays in latency. We show that bradyzoites drastically alter their hosts transcriptional program and this is dependent on the export of parasite proteins across the PVM-cyst wall. Furthermore, we demonstrate that protein export by bradyzoites is critical to protect infected host cells undergoing IFNγ stimulated cell death. Our work provides the first evidence the mechanisms used by latent Toxoplasma that allows for long-term survival and provides an interesting model to understand the differences in host manipulation used by pathogens during acute and chronic-stage infection.